Cyanide poisoning in Taiwan

Development of a biomimetic sensor for selective identification of cyanide

“…All the chemicals used were of analytical or HPLC grade. The cobalt II 1,2,3,4,8,9,10,11,15,16,17,18,22,23,24,25-hexadeca-uoro-29H,31H-phthalocyanine complex, cyanide, mineral oil and graphite powder were purchased from Sigma-Aldrich. NaH 2 PO 4 , H 3 BO 3 and NaOH were purchased from Synth-Bra-zil®.…”

“…Cyanide is an extremely toxic ion readily absorbed by living organisms through inhalation, oral and dermal routes of exposure. The acute toxic effects of ingestion or inhalation of cyanide from suicide or homicide attempts [1][2][3][4][5] are generated by the process whereby cyanides transfer through the blood and then bind to ferric iron of cytochrome oxidase, inhibiting electron transport and disrupting cells from their use of oxygen, 6,7 and then leading to vomiting, convulsion, loss of consciousness, and eventually death. [8][9][10][11][12][13] Fatal oral doses for adults are 0.2 g for cyanide potassium and 0.3 g for cyanide sodium, and 1.2-5 mg kg À1 for children.…”

“…This paper describes the development and application of a simple, cheap and environmentally friendly method for the rapid determination of cyanide in drinking water and river water samples. A voltammetric sensor based on a carbon paste electrode is modied using the cobalt II 1,2,3,4,8,9,10,11,15,17,18,22,23,24,25-hexadecauoro-29H,31H-phthalocyanine complex, a potential biomimetic catalyst of the P450 enzyme for the sensitive and selective quantication of cyanide.…”

Distribution of cyanide in heart blood, peripheral blood and gastric contents in 21 cyanide related fatalities

“…The acute toxic effects of an ingestion or inhalation of cyanide from suicide or homicide attempts [4][5][6][7][8], or of inhalation of combustion gas in a fire [9,10] are generated by the process whereby cyanides transferred through the blood and then bound to ferric iron of cytochrome oxidase inhibit electron transport and disrupt cells in their use of oxygen, resulting in hypoxia and physiological function suppression [11,12]. This is an intracellular poison by cyanide intoxication, which occurs because most of the cyanides in blood are concentrated in the red blood cells and bound to methemoglobin.…”

Cyanide: an unreported cause of neurological complications following smoke inhalation

“…In fire victims, a fixed 5 g dose (equivalent to approximately 3.71 mmol) of hydroxocobalamin can wholly bind cyanide in blood cyanide concentrations up to 40 µmol/l 27. Recently, Hung et al reported a case of severe cyanide poisoning initially treated with a 2.5 g dose of hydroxocobalamin 28. This suboptimal dose resulted in partial reversal of lactic acidosis, and it was only after an additional 2.5 g dose was administered that complete recovery ensued.…”